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S. Nakao, M. Miura, Y. Hata, T. Ishibashi; Dexamethasone Inhibits IL–1ß–Induced Neovascularization in Mouse Cornea . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1625.
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© ARVO (1962-2015); The Authors (2016-present)
Dexamethasone, a member of corticosteroids, is a potent anti–inflammatory drug which is used in the treatment of various eye diseases. The expression of IL–1ß which is an angiogenic factor as well as an inflammatory cytokine increases in various corneal diseases. The purpose of the present study was to investigate the effect of dexamethasone on IL–1ß–induced corneal neovascularization.
IL–1ß was implanted in murine corneas with or without treatment of dexamethasone and the angiogenic response was investigated on day 6. The expression of VEGF, KC, or MIP2 protein in IL–1ß–implanted corneas was analyzed by ELISA on days 2, 4, and 6. The infiltration of CD11b(+)Gr–1(+) or CD11b(+)F4/80(+) cells into IL–1ß–implanted cornea was examined by FACS analysis on day 4.
Dexamethasone could inhibit IL–1ß–induced corneal neovascularization. The expression of VEGF, KC and MIP–2 in corneas were increased by IL–1ß implantation. Both the induction of VEGF and KC by IL–1ß were inhibited by dexamethsone on day 2. However, MIP–2 expression could not be inhibited by dexamethsone. The infilatration rate of neither CD11b(+)Gr–1(+) nor CD11b(+)F4/80(+) cells on day 4 also could be affected by dexamethasone significantly.
Dexamethasone exerted an angiostatic effect on IL–1ß–induced corneal neovascularization. The inhibitory effect was via inhibition of VEGF and KC expression but not blockage of inflammatory cell infiltration.
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